Human resting extracellular heat shock protein 72 concentration decreases during the initial adaptation to exercise in a hot, humid environment

Faculty of Science, University of Strathclyde, Glasgow, Scotland, United Kingdom
Cell Stress and Chaperones (Impact Factor: 3.16). 02/2006; 11(2):129-34. DOI: 10.1379/CSC-158R.1
Source: PubMed


Heat shock protein (Hsp) 72 is a cytosolic protein that also is present in the circulation. Extracellular Hsp72 (eHsp72) is inducible by exercise and is suggested to act as a danger signal to the immune system. The adaptive response of eHsp72 to repeated exercise-heat exposures in humans remains to be determined. An intracellular animal study found a reduced Hsp72 response, with no change in resting levels, during heat stress after a single day of passive heat acclimation. The current study therefore tested whether adaptations in human eHsp72 levels would similarly occur 24 hours after a single exercise-heat exposure. Seven males completed cycle exercise (42.5% V(O2peak) for 2 hours) in a hot, humid environment (38 degrees C, 60% relative humidity) on each of 2 consecutive days. Blood samples were obtained from an antecubital vein before exercise and 0 hours and 22 hours postexercise for the analysis of eHsp72. Exercise-heat stress resulted in enhanced eHsp72, with a similar absolute increase found on both days (day 1: 1.26 ng/mL [0.80 ng/mL]; day 2: 1.29 ng/mL [1.60 ng/mL]). Resting eHsp72 decreased from rest on day 1 to day 2's 22-hour postexercise sample (P < 0.05). It is suggested that the reduction in resting eHsp72 after 2 consecutive exercise-heat exposures is possibly due to an enhanced removal from the circulation, for either immunoregulatory functions, or for improved cellular stress tolerance in this initial, most stressful period of acclimation.

Download full-text


Available from: Myra Nimmo
  • Source
    • "Lifestyle factors, especially unhealthy eating patterns, might affect human health [14, 15]. The effect of exposure to humidity on immune function has been identified, and several studies have shown that humidity stress is associated with suppression of several T-cell functions and defective immune response [4–6, 16, 17]. The molecular mechanism leading to humidity-induced immunosuppression is obscure. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Environmental dampness is one factor which can cause human diseases. The effects of exposure to humidity on human immune function are diverse and numerous. In the theory of traditional Chinese medicine (TCM), dampness is defined as one of the major pathogenic factors in the human body. It is divided into "external dampness" and "internal dampness." However the molecular mechanism leading to humidity-induced immunosuppression is obscure. In the present study, we investigated the expression of the T-cell antigen receptor variable β (TCRVβ) subfamilies in rats which were fed in different humid environment. And the expression levels of the TCRVβ subfamilies were detected using FQ-PCR. We found that the dampness might reduce the immunological recognition function of rats. And the obstruction of the immunological recognition function might be caused by internal dampness rather than external dampness.
    Full-text · Article · May 2014 · Evidence-based Complementary and Alternative Medicine
  • Source
    • "conditioning, while the acute response to exercise in the heat may be unchanged (Marshall et al., 2006). Therefore, we also sought to provide further information on the HSR in humans. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Most heat acclimation data are from regimes longer than 1 week, and acclimation advice is to prevent dehydration. Objectives: We hypothesized that (i) short-term (5-day) heat acclimation would substantially improve physiological strain and exercise tolerance under heat stress, and (ii) dehydration would provide a thermally independent stimulus for adaptation. Methods: Nine aerobically fit males heat acclimated using controlled-hyperthermia (rectal temperature 38.5°C) for 90 min on 5 days; once euhydrated (EUH) and once dehydrated (DEH) during acclimation bouts. Exercising heat stress tests (HSTs) were completed before and after acclimations (90-min cycling in Ta 35°C, 60% RH). Results: During acclimation bouts, [aldosterone]plasma rose more across DEH than EUH (95%CI for difference between regimes: 40-411 pg ml(-1) ; P = 0.03; n = 5) and was positively related to plasma volume expansion (r = 0.65; P = 0.05), which tended to be larger in DEH (CI: -1 to 10%; P = 0.06; n = 9). In HSTs, resting forearm perfusion increased more in DEH (by 5.9 ml 100 tissue ml(-1) min(-1) : -11.5 to -1.0; P = 0.04) and end-exercise cardiac frequency fell to a greater extent (by 11 b min(-1) : -1 to 22; P = 0.05). Hydration-related effects on other endocrine, cardiovascular, and psychophysical responses to HSTs were unclear. Rectal temperature was unchanged at rest but was 0.3°C lower at end exercise (P < 0.01; interaction: P = 0.52). Conclusions: Short-term (5-day) heat acclimation induced effective adaptations, some of which were more pronounced after fluid-regulatory strain from permissive dehydration, and not attributable to dehydration effects on body temperature. Am. J. Hum. Biol., 2014. © 2014 Wiley Periodicals, Inc.
    Full-text · Article · May 2014 · American Journal of Human Biology
  • Source
    • "cardiovascular stability; reduced core temperature at rest and during exercise; more rapid sudomotor onset and efficiency, etc.) (Garrett et al. 2011). The response of eHsp72 to environmental factors has not been uniform , with significant increases (Whitham et al. 2007; Yamada et al. 2007; McClung et al. 2008; Magalhães et al. 2010; Périard et al. 2012), or no change (Marshall et al. 2006; Watkins et al. 2007; Hom et al. 2012) from rested basal values reported. Exercise-heat stress research has largely implemented experimental designs where exogenous (external) factors of exercise intensity and exercise-heat stress conditions are controlled to elicit and measure changes in endogenous (internal) response. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Extracellular heat shock protein 72 (eHsp72) concentration increases during exercise-heat stress when conditions elicit physiological strain. Differences in severity of environmental and exercise stimuli have elicited varied response to stress. The present study aimed to quantify the extent of increased eHsp72 with increased exogenous heat stress, and determine related endogenous markers of strain in an exercise-heat model. Ten males cycled for 90 min at 50 % \( \overset{\cdot }{\mathrm{V}}{\mathrm{O}}_{2\mathrm{peak}} \) in three conditions (TEMP, 20 °C/63 % RH; HOT, 30.2 °C/51%RH; VHOT, 40.0 °C/37%RH). Plasma was analysed for eHsp72 pre, immediately post and 24-h post each trial utilising a commercially available ELISA. Increased eHsp72 concentration was observed post VHOT trial (+172.4 %) (p < 0.05), but not TEMP (−1.9 %) or HOT (+25.7 %) conditions. eHsp72 returned to baseline values within 24 h in all conditions. Changes were observed in rectal temperature (T rec), rate of T rec increase, area under the curve for T rec of 38.5 and 39.0 °C, duration T rec ≥ 38.5 and ≥39.0 °C, and change in muscle temperature, between VHOT, and TEMP and HOT, but not between TEMP and HOT. Each condition also elicited significantly increasing physiological strain, described by sweat rate, heart rate, physiological strain index, rating of perceived exertion and thermal sensation. Stepwise multiple regression reported rate of T rec increase and change in T rec to be predictors of increased eHsp72 concentration. Data suggests eHsp72 concentration increases once systemic temperature and sympathetic activity exceeds a minimum endogenous criteria elicited during VHOT conditions and is likely to be modulated by large, rapid changes in core temperature.
    Full-text · Article · Oct 2013 · Cell Stress and Chaperones
Show more